Fleming and the Problem of Contamination?

In 1928, Alexander Fleming, a Scottish bacteriologist working at St. Mary's Hospital in London, cultivated a series of culture plates of Staphylococcus bacteria as part of his ongoing research into bacterial pathogenesis. Following an interruption in his work during an August vacation, Fleming returned to his laboratory to find that several of his plates had become contaminated with mold. Standard practice in that era, and indeed in Fleming's own laboratory protocol, was to discard contaminated cultures without detailed examination, as contamination was considered a failure of technique and the plates themselves were assumed to be no longer useful for study. Fleming discarded these plates in the ordinary waste.

The contaminated cultures contained Penicillium mold, which produces compounds with bacteriostatic and bactericidal properties against Staphylococcus and related organisms. In other historical circumstances, the observation of this antagonism would later be recognized as a landmark discovery with profound consequences for twentieth-century medicine. Ernest Duchesne, a French military physician, had documented similar antagonistic interactions between Penicillium and bacterial growth in 1897 but died in 1912 before his observations gained traction in the scientific community; his work remained unpublished and was not repeated by other researchers. Fleming's unexamined plates thus represented a second lost opportunity to establish the systematic study of mold-derived bacterial antagonism.

The disposal of these plates occurred at a moment when the medical world had just begun to recognize the limitations of existing systemic antibacterial therapy. The azo drugs, sulfonamide compounds, had not yet been synthesized. The dominant treatments for systemic bacterial infection remained supportive care, passive immunotherapy through serum therapy derived from animal antitoxins, and increasingly desperate surgical intervention. By the early 1930s, as Bayer AG and other chemical manufacturers began to develop and market the first azo drugs, the absence of a well-developed chemical antimicrobial class had already begun to reshape medical thinking. The field had not yet crystallized around prevention and containment, but the infrastructure of that response—institutional focus on asepsis, careful attention to surgical technique, and investment in passive immunity—was already developing.

The historiographical record of Fleming's 1928 contamination is sparse. Fleming himself published no account of the contaminated plates. St. Mary's Hospital kept no detailed record of the incident. The plates themselves were discarded as waste and have never been located. Historians of bacteriology have subsequently reconstructed the episode from Fleming's later autobiographical statements, some made in interviews conducted decades after the event, and from the known facts of his work schedule and laboratory practice in that period. Malcolm Macmillan's examination of Fleming's own records and his interviews with Fleming in the 1960s established the basic chronology: a series of plates, left on the bench during Fleming's holiday in August 1928, returned contaminated, and then destroyed according to ordinary laboratory practice.

What remains uncertain is whether Fleming noticed the contamination before discard. Some accounts suggest that he observed the plates but saw no particular significance in the antagonistic effect. Others hold that the plates were discarded by junior laboratory staff without Fleming's direct examination, a practice consistent with the hierarchical organization of that period's bacteriology laboratories. The distinction matters for understanding the history of twentieth-century medicine, because it determines whether Fleming made an active choice to discard an unremarkable result or whether a potentially significant observation passed through his laboratory entirely unnoticed. Historians have proposed both interpretations, and the archival evidence permits neither to be ruled out conclusively.

By the time Fleming achieved recognition for his later work on bacterial lysozyme and on the comparative growth rates of Staphylococcus strains, the medical world had already begun to reorganize itself around the premise that systemic bacterial infection could not be reliably cured by chemical means. The invasion of Sicily in 1943 and the subsequent Norman campaign demonstrated this reality with terrible clarity, as gangrene and systemic sepsis deaths mounted to rates incompatible with continued reliance on azo drugs as a primary medical tool. By 1952, when the international community formally adopted asepsis maximalism as the coordinated response to untreatable bacterial infection, Fleming's lost opportunity had already been overtaken by institutional reality. The paper plates and the mold antagonism had become historically irrelevant—not because they had been evaluated and found wanting, but because they had never entered the record at all.

The disposal of Fleming's plates in 1928 stands as a point of divergence not because it was unusual in its moment, but because it foreclosed what might have followed. Had the contamination been carefully examined, had the antagonistic effect been recognized and pursued, had resources been allocated to the systematic study of mold-derived compounds in the 1930s rather than to chemical synthesis, the medical history of the twentieth century would have followed a different course. The path of asepsis maximalism, the vast infrastructure of prevention that now structures hospital design and public health, the societal reorganization around bacterial containment rather than cure—all of these emerged not from Fleming's lost observation, but from its permanent absence.